Measurement and implications of the Q˙s/Q˙t

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Measurement and implications of the images/imaget

Robert A. Strickland, MD

Hypoxemia can be caused by a variety of factors (Box 32-1). This chapter will focus on the primary cause of hypoxemia—shunting, which may, at times, be due to ventilation/perfusion (image/image) mismatch.

Ventilation/perfusion mismatch

Ideally, pulmonary perfusion (image) evenly matches alveolar ventilation at all levels of the lung; however, perfect matching does not occur because the distribution of ventilation and perfusion and the image/image ratio vary throughout the lung. A normal lung has a image/image ratio of approximately 0.8. A image/image ratio of 0 (i.e., a shunt) exists when perfused alveoli have no ventilation and the values for PO2 and PCO2 of the trapped air are the same as those of mixed venous blood (PO2 = 40 mm Hg and PCO2 = 47 mm Hg). Conversely, a image/image ratio of ∞ exists when ventilated alveoli have no perfusion and, at sea level, the PO2 and PCO2 equal approximately 150 and 0 mm Hg, respectively. Nonperfused alveoli (i.e., alveolar dead space) is approximately 25 to 50 mL in a healthy 70-kg person. Figure 32-1 depicts the progression of a image/image ratio from 0 to ∞; the normal, idealized, alveolar-capillary unit is shown as example A.

In contrast with blood vessels in all other tissues, which dilate in response to hypoxemia, the blood vessels of intact lung constrict in response to hypoxia (termed hypoxic pulmonary vasoconstriction [HPV]). Blood flow is directed away from poorly ventilated regions of a lung to better ventilated lung fields. Thus, the overall image/image ratio improves, better oxygenating blood. A low PO2 in the pulmonary arteries and pulmonary capillaries is the predominant stimulus that produces HPV, although a low mixed venous O2 pressure (PimageO2) also plays a role. A PO2 below 100 mm Hg will initiate HPV; marked vasoconstriction occurs with a PO2 less than 70 mm Hg, becoming progressively more severe as PO2 levels continue to decrease. The mechanism for HPV is not well understood, but it appears that pulmonary vascular endothelium responds to a low O2 tension, with endothelium-derived vasoconstrictor biochemicals (e.g., leukotrienes and prostaglandins) constricting arteriolar smooth muscle.

A variety of physiologic alterations and pharmacologic interventions alter HPV. Respiratory acidosis and metabolic acidosis increase HPV, whereas respiratory alkalosis and metabolic alkalosis decrease HPV. In vitro studies have shown that inhaled anesthetic agents uniformly inhibit HPV, but the results of in vivo studies have not often yielded clinically significant effects. Systemically administered vasodilators, such as nitroprusside and nitroglycerin, generally adversely affect HPV, which may be of consequence in patients with significant obstructive lung disease or during one-lung ventilation.

Shunting due to other causes

A small fraction of blood in the cardiac output, normally 2% to 5%, enters the arterial circulation without first passing through the pulmonary circulation, accounting for the normal O2 alveolar-arterial gradient P(A-a)O2. The causes for this type of venous admixture include (1) the thebesian veins, which drain blood from the coronary circulation directly into the left atrium and, rarely, the left ventricle and (2) the bronchial vein, which provides the nutritive perfusion of the bronchial tree and pleura. Abnormal anatomic shunts include right-to-left atrial and ventricular septal defects and pulmonary arteriovenous malformations.

Hypoxemia that is the result of a physiologic or anatomic shunt cannot be corrected by having the patient breathe supplemental O2. The hemoglobin in blood that perfuses alveoli with a image/image ratio of 1 will readily achieve 100% saturation; increasing the partial pressure of O2 in these alveoli will minimally increase the O2 content. Blood that perfuses alveoli with a image/image ratio of 0 will not be exposed to any O2, no matter the fraction of inspired O2 (FIO2); therefore, no significant improvement in arterial oxygenation occurs (Figure 32-2).

As previously stated, the normal shunt fraction is less than 5%. Clinically significant shunts equal 10% to 20% of cardiac output, whereas potentially fatal shunts are usually greater than 30%. Seldom does a shunt result in an elevated PaCO2. Chemoreceptors sense elevations in PaCO2 and increase ventilation. The PaCO2 of unshunted blood is reduced, and the overall PaCO2 is usually normal. If ventilatory drive related to a low PaO2 produces significant hyperventilation, it is possible to actually have a PaCO2 that is less than normal.

Calculation of shunt fraction

The fraction of cardiac output that passes through the various shunts is expressed as the shunt fraction (images/imaget):

< ?xml:namespace prefix = "mml" />Q˙s/Q˙t = (CcO2CaO2)/(CcO2CvO2)

image

where Cc equals the O2 content of end-pulmonary capillary blood, Ca is the O2 content of arterial blood, and Cimage represents the O2 content of mixed venous blood. The O2 content of arterial blood is calculated by:

Ca = 1.39(hemoglobin concentration) (% O2saturation) + 0.003(PaO2)

image

The O2 contents of Cc and of Cimage are calculated by inserting the respective O2 saturation and PaO2 values into the equations.

When cardiac output and hemoglobin concentration are normal and the PaO2 is greater than 175 mm Hg, the shunt fraction can be estimated by using the simplified formula:

P(A−a)O220

image